Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5857924 | Reproductive Toxicology | 2016 | 9 Pages |
Abstract
We recently demonstrated that acetylcholine (ACh) produced reliable vasoconstrictions in the umbilical cords. This study investigated the possible mechanisms with different antagonists. ACh-mediated vasoconstrictions were decreased by voltage-operated calcium (Ca2+) channels antagonist nifedipine or inositol-1,4,5-trisphosphate-mediated Ca2+ release antagonist 2-aminoethyl diphenylborinate, indicating that both extracellular and intracellular calcium modulated the ACh-stimulated umbilical contraction. Intracellular Ca2+ concentrations were increased simultaneously with vasoconstrictions by ACh in the umbilical vessels. Inhibiting large-conductance calcium-dependent potassium (BK) channels enhanced ACh-mediated contraction, whereas inhibiting voltage dependent potassium (K+), inward rectifier K+ and ATP-sensitive K+ channels had no effects. Incubation with specific K+ channel inhibitors showed that ACh suppressed BK currents rather than 4-aminopyridine-sensitive K+ channels currents. The results suggested that blood vessels in umbilical cords had special characteristics in response to cholinergic signals. ACh-stimulated umbilical vasoconstrictions were mediated via muscarinic receptor subtype 1/3-protein kinase C/cyclooxygenase-BK channel pathways.
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Authors
Zhoufeng Zhu, Jiaqi Tang, Xiuwen Zhou, Sharon Xiang, Xiaolin Zhu, Na Li, Ruixiu Shi, Yuan Zhong, Lubo Zhang, Miao Sun, Zhice Xu,